Heart failure (HF) is the leading cause of cardiovascular morbidity and mortality worldwide. About half of heart failure patients have heart failure with preserved ejection fraction (HFpEF). Distinct from traditional HF, i.e., heart failure with reduced ejection fraction in which the ventricle cannot contract, patients with HFpEF show declined performance of heart ventricle, not at the time of contraction, but during the phase of diastole. HFpEF patients show normal ejection fraction of blood pumped out of the ventricle, but the heart muscle does not quickly relax to allow efficient filling of blood returning from the body. Morbidity and mortality of HFpEF are similar to traditional HF; however, therapies that benefit traditional HF are less effective in treating or preventing HFpEF.
One of the causes of diastolic dysfunction (diastolic heart failure) can be cardiac fibrosis.
For people with chronic kidney disease (CKD) and advancing severe renal impairment or ESRD, salvage of the native kidney is not a tangible goal with treatment options limited to renal transplantation or dialysis. However, these individuals are also at markedly increased risk of other comorbidities that themselves may remain amenable to therapeutic interventions. Among these comorbidities, heart failure, especially heart failure with preserved ejection fraction (HFpEF) is particularly common, where it carries a mortality risk equivalent to that of systolic heart failure, but has no evidence-based treatment.
HFpEF may affect up to 70% of the dialysis population. Unfortunately, whereas ACE inhibitors and angiotensin II receptor blockers represent established evidence-based therapies for the treatment of either systolic heart failure or CKD they provide little if any benefit in the treatment of HFpEF.